The present study examined the role of reversion-inducing cysteine-rich protein with Kazal motifs (RECK) promoter hypermethylation as a causative factor in metastasis of osteosarcoma. Using human pathological samples, it is demonstrated that RECK, a cysteine protease that reversibly regulates expression of matrix metalloproteases like matrix metallopeptidase 9 (MMP9), is transcriptionally inhibited in osteosarcoma, especially metastatic variants. This result comes from its promoter hypermethylation, as evaluated in the present study by methylation-specific PCR reaction. The expression of RECK was also significantly diminished in the metastatic variants of osteosarcoma. This downregulation of RECK in advanced grades of osteosarcoma and metastatic grades was also associated with the increased expression of invadosome-specific markers like MMP9, phospho-FAK, and integrins, suggesting the complex contributions of RECK in the prevention of metastasis and its downregulation as a causative factor in osteosarcoma metastasis.

Background: Osteosarcoma (OSA), the most common primary bone malignancy, is characterized by a wide spectrum of complicated pathologies and frequent distal metastasis and causes death in adolescents and young adults worldwide. Antitumor drug treatment strategies include various cytotoxic chemotherapy drugs, while molecular targeted therapy for OSA is currently less used. The present work revealed the role played by the miR-596/Survivin axis in affecting the sensitivity of OSA cells to anlotinib, a novel molecular targeting agent. Methods: By virtual screening, we found that miR-596 might target Survivin by using an online tool (miRDB). RNA levels of miR-596 and Survivin in clinical specimens were examined with qPCR. The effect of miR-596 on anlotinib's antitumor effect was examined with MTT experiments, the subcutaneous tumor model, or the intramuscular tumor model. Results: Overexpression of miR-596 via lentiviral particles repressed the protein level of Survivin in U2OS cells. Transfection of miR-596 enhanced the antitumor effect of anlotinib on U2OS cells or five cell lines derived from OSA patients. Conclusion: miR-596 targets Survivin and enhances the antitumor effect of anlotinib on OSA cells.

Objective. To investigate the clinical efficacy of different acupuncture points in the treatment of ankylosing spondylitis with supervised moxibustion. Methods. Retrospective analysis of 61 AS patients (diagnosed as ankylosing spondylitis of kidney-yang deficiency type by Chinese medicine) admitted to our hospital from January 2020 to February 2021, randomly divided into 30 cases in the experimental group (Du moxibustion + basic western medicine treatment) and 31 cases in the control group (basic western medicine treatment alone). The changes in quantitative scores of the main symptoms and major signs (thoracic mobility, occipital-wall distance, finger-ground distance, and laboratory index (ESR)) were analyzed before and after treatment. Results. Of the 30 cases in the experimental group, 2 were clinically cured, 3 were apparently effective, 21 were effective, and 4 were ineffective, with an overall effective rate of 86.7%; of the 31 cases in the control group, 1 was clinically cured, 1 was apparently effective, 1 was effective. 24 were effective, and 5 were ineffective, with an overall effective rate of 83.9%. Comparing the efficacy by t-test, P < 0.05 , indicating that the effect of Du moxibustion + Western medicine treatment was better. Conclusion. The treatment of ankylosing spondylitis with kidney-yang deficiency by moxibustion + western medicine can improve the efficacy, alleviate the inflammatory response and improve the patient’s symptoms and signs, and immune indexes.

Objective To explore the effects of hypoxic preconditioning neural stem cell (P-NSC) transplantation on rats with spinal cord injury (SCI). Methods After identification, the NSCs were treated with hypoxic preconditioning. The NSCs migration was detected by Transwell method. RT-qPCR was used to detect the mRNA levels of HIF-1α, CXCR4 in NSC. The secretion of representative neurotrophic factors (VEGF, HGF, and BDNF) was checked by Western blot. Forty-six SCI rats were randomly divided into three experimental groups: SCI group (PBS injection, n = 10); N-NSC group (NSC atmospheric normoxic pretreatment injection, n = 18); and P-NSC group (NSC ’s hypoxic preconditioning injection, n = 18). The sham operation group was also included (rats underwent laminectomy but not SCI, n = 10). The recovery of hindlimb motor function was evaluated by BBB score. The level of spinal cord inflammation (IL-1β, TNF-α, and IL-6) was determined by ELISA. Western blot was used to detect the content of TMIGD1 and TMIGD3 in spinal cord. Results Compared with the N-NSC group, the number of NSC-passing membranes in the P-NSC group increased with the increase of the culture time ( p < 0.05). Compared with N-NSC, P-NSC had higher levels of VEGF, HGF, and BDNF after 1 week of culture ( p < 0.05). The BBB score of the P-NSC group was significantly higher than that of the N-NSC group at 7 and 28 days ( p < 0.05). Compared with the SCI group, the levels of TNF-α, IL-1β, and IL-6 were significantly reduced after NSC treatment, and the P-NSC group was lower than the N-NSC group ( p < 0.05). Compared with the SCI group, the levels of TMIGD1 and TMIGD3 increased. Compared with the N-NSC group, and the levels of TMIGD1 and TMIGD3 increased in the P-NSC group ( p < 0.05). Conclusion P-NSC administration could improve SCI injury, and the levels of TMIGD1 and TMIGD3.